The proposed studies are designed to test the hypothesis that there are natural anti-inflammatory mechanisms which suppress urate crystal induced inflammation by investigating the mechanisms of natural and pharmacologic termination of the acute attack of gout and the physiologic conditions in which urate crystals are rendered non-phlogistic. The contribution of changes in the crystal, synovial fluid constituents and the phagocytic cell will be studied. The effects of synovia fluid obtained from "non-inflamed" joints during subsiding attacks of gout on random and directed migration, adherence, phagocytosis, and enzyme release by granulocytes will be determined. The ability of fluid to inhibit the inflammatory activity of synthetic urate crystals as assessed by complement activiation, formation of serum derived and cell derived chemotacpic factors, phagocytsis, and enzyme release by phagocytic cells will be assessed. The specific factors in synovial fluid responsible for any effects will be assessed. The role of prostaglandins and related inflammatory lipids including changes in production of specific lipids in modulation of urate crystal induced inflammation will be investigated by determining concentrations in synovial fluid, assessing the effects of addition of specific inflammatry lipids on granulocyte function, and by assessing the effects of synovial fluid constituents on the ability of urate crystals to stimulate granulocyte release of these lipids.